Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of C-myc proto-oncogene were studied at the levels of protein in bone marrow cells obtained from patients with AML and CML. It was found that the expression of C-myc in florid AML and during blast phase of CML were much higher than that in remission of AML and in chronic phase of CML. In 7 cases of AML diagnosed for the first time, 2 cases with high C-myc expression had no remission after 3-6 months, while 5 with rare C-myc expression had remission after 3-6 months. This results suggest that the expression of C-myc proto-oncogene are possibly sensitive indicator of the prognosis of leukemia.
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PMID:[The expression of C-myc oncogene in leukemia and its relationship to clinical symptoms]. 139 24

We describe the clinicomorphological features in 33 cases of primary myelodysplastic syndrome classified according to the FAB classification which presented to a single centre over a 12 year period. Presenting features were typically related to pancytopenia although hepatosplenomegaly and granulocytic sarcomas were far more prevalent than in the adult population. Morphological assessment of the peripheral blood and the bone marrow showed seven patients had refractory anaemia (RA), 13 patients had RA with excess of blasts (RAEB), nine patients had RAEB in transformation (RAEB-t) and four patients had chronic myelomonocytic leukaemia (CMML). The overall mean survival was short (9.9 months) in all the subgroups and the leukaemic transformation rate was high. None of the patients scored 0-1 according to the Bournemouth Scoring System; four patients scored 2 whereas 29 patients scored 3 to 4. We conclude that unlike adults, the myelodysplastic syndromes in children run an aggressive clinical course, irrespective of the FAB subtype, and the pathogenesis of these diseases in paediatric practice warrants scientific scrutiny. Intensive chemotherapy such as the one used in de novo-AML lead to complete remission in some children and these early results suggest that this should be the treatment of choice in paediatric MDS.
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PMID:Primary myelodysplastic syndrome in children: the clinical experience in 33 cases. 141 17

Following i.v. bromodeoxyuridine infusion, a double-label technique using in vitro tritiated thymidine was used to determine the labeling index (LI), duration of S-phase (Ts), and cell cycle time (Tc) in pediatric leukemia patients. Eleven patients with acute lymphoblastic leukemia (ALL) and six patients with acute nonlymphoblastic leukemia (ANLL) were studied. Results of cell cycle kinetic studies are given for each group. Although median values for AML and ALL patients are similar to values reported in previous studies, there is a wide range of values among individual patients. The variation among the kinetic properties of blast cells in these patients reflects the heterogeneity of the acute leukemias of childhood. Further studies will be done to determine if these parameters correlate with outcome of therapy for pediatric leukemia patients.
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PMID:In vivo cell cycle characteristics of pediatric leukemia patients. 142 98

Occupational causes of cancer are difficult to establish because of the long latency period and difficulty in identifying occupational linkages. This study provides a regional analysis of cancer incidence and mortality as a method of identifying localizing factors in cancer that can be followed by more specific epidemiologic investigation. In this study we analyze the regional standardized mortality ratios (SMRs) for site-specific cancers, by age, sex and continent of birth for the years 1983-86, for the Jewish population of Israel. Elevated total malignant and benign neoplasm SMRs were found in Acre (SMR 109, P < 0.05), Haifa (104, P < 0.05) and Tel Aviv (107, P < 0.001). The only other statistically significantly elevated SMRs were found in Acre for lung cancer (133, P < 0.05) and leukemia (171, P < 0.05). Age and sex-standardized incidence ratios (SIRs) by regions are also presented for the years 1980-81 for the Jewish population. Haifa had elevated SIRs for colorectal cancer (126, P < 0.001), breast cancer (118, P < 0.01) and lymphomas (126, P < 0.05). Elevated lung cancer SIRs were found in both Acre (145, P < 0.05) and Ramla (143, P < 0.05). Male to female incidence ratios (MFIRs) for ages 30+ for the Israeli Jewish population are also presented. Elevated bladder cancer MFIRs were found in the heavily industrialized Haifa region (7.69 vs. 4.62 P < 0.05). For Ramla residents, bladder and oronasopharyngeal cancer MFIRs were approximately three times the national average (not statistically significant). Ramla also had elevated MFIRs for lung cancer (14.9 vs. 3.4 nationally, P < 0.01), as did Acre (7.6 vs. 3.4 nationally, P = 0.06). These elevated MFIRs are suggestive of occupational exposure from the cement and asbestos factories in the Ramla and Acre regions. Regional analyses of cancer mortality and cancer incidence (using SMRs, SIRs and MFIRs) can serve as a basic tool for identifying sentinel markers of excess rates. Our findings indicate regions where we should undertake case-referent studies in order to identify potential risk factors and where to target possible preventive programs.
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PMID:Regional differences in cancer incidence and mortality in Israel: possible leads to occupational causes. 142 7

Two patients with acute myeloblastic leukemia with t(6;9)(p23;q34) translocation and classified as AML-M2 relapsed as acute monocytic leukemia (AML-M5). Trisomy 8 was found associated with t(6;9) at that time in both patients. Such changes in differentiation of leukemic cells have not previously been reported in this subtype of AML and add data favoring the pluripotent nature of the stem cell involved in leukemia with t(6;9).
Leukemia 1992 Nov
PMID:Relapse as acute monoblastic leukemia (AML-M5) of t(6;9) acute myeloblastic leukemia (AML-M2). 143 8

The study combines the effects of prolonged postremission chemotherapy with that of very early intensification. 900 adult patients at all ages with newly diagnosed AML uniformly received TAD for induction and consolidation followed by monthly myelosuppressive maintenance for 3 years. In patients of 60+ years with persistent bone marrow blasts a second TAD course was given. In all patients of less than 60 years a second induction course started on day 21 even in aplasia with no blasts. Second induction was randomly either TAD or HAM. In the younger age group 69% attained CR and similar in the two arms the CR rate after 5 years is 35%. Including the 50% patients attaining CR in the higher age group the CR rate after 5 years is 32%. In 40 patients receiving allogeneic BMT and 21 patients receiving autologous BMT in first CR relapse free survival is similar to that from chemotherapy alone in a matched pair analysis. We conclude that age adapted very early intensification followed by prolonged postremission chemotherapy represents a therapeutic progress.
Leukemia 1992 Nov
PMID:Combined effect of very early intensification and prolonged post-remission chemotherapy in patients with AML. 143 38

The human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origin and spread of human leukemia. 143 86

We have performed a retrospective analysis of the clinical, morphologic, and cytogenetic findings in 26 patients diagnosed between January 1969 and September 1991 with acute erythroblastic leukemia de novo (EL or AML-M6). Clonal chromosomal abnormalities were found in 20 (77%) patients (95% confidence interval [CI], 61% to 93%). Loss of all or part of the long arm (q) of chromosomes 5 and/or 7 was observed in 17 (65%) patients (95% CI, 47% to 83%). In addition, the karyotypes were often complex, with multiple abnormalities and subclones. Among the remaining nine patients, six had a normal karyotype and one each had trisomy 8, t(3;3), or t(3;5). The overall frequency of abnormalities of chromosomes 5 and/or 7 observed in our M6 patients is similar to that observed in our patients with therapy-related acute myeloid leukemia (t-AML; 99 of 129 patients, 77%), but substantially higher than that noted in our other patients with AML de novo (French-American-British [FAB] subtypes M1-M5: 52 of 334 patients, 16%). Our M6 patients with abnormalities of chromosomes 5 and/or 7 were older and had a shorter median survival (16 v 77 weeks [P = .005]) than did the M6 patients without these abnormalities. We found no correlation between morphologic features and either cytogenetic abnormalities or clinical outcome. Of note was the finding that the percentage of myeloblasts, which may account for only a small fraction of the total marrow elements when the revised FAB criteria are applied, had no bearing on prognosis. We conclude that acute erythroblastic leukemia, when defined by morphologic criteria, consists of two distinctive subgroups: one group tends to be older, has complex cytogenetic abnormalities, especially of chromosomes 5 and/or 7, and shares biologic and clinical features with t-AML; the other group, with simple or no detectable cytogenetic abnormalities, has a more favorable prognosis when treated with intensive chemotherapy.
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PMID:Clinical, morphologic, and cytogenetic characteristics of 26 patients with acute erythroblastic leukemia. 145 Apr 12

Loss of a whole chromosome 5 or deletion of 5q are recurring abnormalities in malignant myeloid neoplasms. Chromosomal loss or deletion are the hallmarks of tumour suppressor genes, suggesting that a gene(s) located on 5q may function as a leukaemia suppressor gene. To determine the location of genes on 5q that may be involved in myeloid leukaemogenesis, we examined the breakpoints of the del(5q) in a series of 117 patients with malignant myeloid diseases. By comparing the breakpoints, we identified a small segment of 5q, consisting of band 5q31, that was deleted in each patient. This segment has been termed the critical region. A striking number of genes encoding haematopoietic growth factors have been mapped within or adjacent to the critical region. These include the genes encoding CSF-2, IL-3, IL-4, IL-5 and IL-9. By using fluorescence in situ hybridization, we have refined the localization of these genes to 5q31.1. To facilitate the identification of a tumour suppressor gene on 5q, we are currently preparing a physical map of 5q31. With FISH analysis of a series of cosmid and phage clones, we identified a number of clones within 5q31. By hybridizing these probes to metaphase cells with a del(5q) involving proximal or distal breakpoints within 5q31, we have narrowed the critical region to a small segment of 5q31 containing eight of the cosmids. In addition, we found that the five growth factor genes are excluded from this region. We have used dual colour FISH to determine the order of these cosmids, the order of the known genes mapped to 5q23-33 and the relationship of these genes to the critical region. To date, mutations of these genes in leukaemia cells have not been identified. The clinical features of myeloid diseases associated with a del(5q) are variable (RA 5q- syndrome v. AML); thus, once the involved gene is identified, it will be important to determine whether the same gene is involved in both types of myeloid disorders.
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PMID:Deletions of chromosome 5 in malignant myeloid disorders. 145 Nov 9

Automated platelet counts in a patient with newly diagnosed AML M5 with extreme leukocytosis were reported as 129, 166 and 121 x 10(9)/1. Routine blood films showed a corresponding number of platelet-sized particles, judged to be platelets. The patient was treated for DIC with low-dose heparin infusion. Platelet transfusions were not given initially. The patient died 14 h after admission from intracerebral haematoma. The origin of the platelet-sized particles seen in routine stained blood films was examined by cytochemical and immunological staining for peroxidase, non-specific esterase, CD 13 and CD 33. About 1/3 of the fragments had the same staining characteristics as the leukaemia cells, indicating leukaemia cell origin. Staining for platelet-specific antigen GpIIIa was positive only in 4% of the platelet-sized fragments, with a calculated true platelet count of 4 x 10(9)/1. The presence of cell fragments masquerading as platelets should be suspected in leukaemia patients with bleeding symptoms and normal or near normal platelet counts.
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PMID:Spurious platelet counts in acute leukaemia with DIC due to cell fragmentation. 145 3


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